Role of dexmedetomidine in stress control in traumatic brain injury and its influence on neuroendocrine system

Objective To investigate the role of dexmedetomidine in stress control in moderate and severe traumatic brain injury (TBI) and its influence on neuroendocrine system. Methods Ninety moderate or severe TBI patients (GCS 6-13) were admitted to ICU from May 2009 to January 2012, and they were divided into three groups according to the order of admission. Patients in group A (n=32) received 0.5-1.0μg/kg dexmedetomidine within 30min, maintained with 0.2-0.6μg/(kg.h) dexmedetomidine for 24h, and morphine was administered by intravenous injection when necessary; patients in group B (n=31) received a 0.5-2.0mg/kg loading dose of propofol within 10min, maintained with 1.0-3.0mg/(kg.h) for 72h, and morphine was administered by intravenous injection when necessary; patients in group C (n=27) received an intramuscular injection of pethidine or other optional drugs as control. A comprehensive evaluation was performed using Riker sedation-agitation scale combined with physiological and physical response indicators. The blood pressure, heart rate, respiration, tidal volume, arterial blood gas, plasma cortisol, plasma β-endorphin (β-EP), peripheral WBC count and blood glucose were measured and compared in 3 groups. Results The sedation rate of single-drug (i.e., without morphine administration) in groups A, B and C was 86.7%, 80.6% and 77.8% respectively, and no significant difference was found among 3 groups (P>0.05). The mean arterial blood pressure at 30 min after administration was lower than that before administration in group A (P0.05). The WBC count and plasma cortisol level at 24h after treatment were lower than those before administration of the drugs in group A (P0.05). Conclusions Dexmedetomidine could alleviate the stress as a result of moderate and severe TBI, and its anti-stress and sedative effects were similar to those of propofol, but it is necessary to monitor the blood pressure. β-EP may play a coordinating role in the early stage of effect of dexmedetomidine. DOI: 10.11855/j.issn.0577-7402.2013.11.011